Revised concepts of atherogenesis
Keith G. McCullagh, Ph.D., B.V.Sc., M.R.C.V.S.
Department of Pathology, University of Bristol England and Division of Research
More than 20 years ago Page1 reported on the supposed causes of atherosclerosis. Most of the investigators in this field are no longer “new and quite shiny.” They have toiled long and diligently and communicated with each other profusely, and yet “cures” for atherosclerosis have not been proclaimed at least twice a year as Page had expected. That is not to say that knowledge has not advanced in the past 2 decades. The recognition of the major importance of this disease process has attracted many new investigators. Publications have been prolific and newer technology has added sophistication to old experiments. Yet few advances have been of sufficient magnitude to excite the attention of the clinician, surgeon, or pathologist with other areas of interest. Instead, advances in understanding atherosclerosis have been subtle and complex, as is the disease itself.
There are several reasons why this should be so. For one, arteries tend to react to a wide variety of injurious or inflammatory stimuli with a rather uniform set of responses, so that divining the nature of the stimulus from an examination of the lesion, always a hazardous process for the pathologist, no longer has any credibility in degenerative arterial disease. For another, atherosclerosis is a disease which many assume takes a lifetime to develop to the stage where clinically significant occlusion of an artery occurs (Fig. 1). During that lifetime, the artery may have been subjected to many stimuli. Even if a full history of these influences were available, attempts to . . .